Chorea Caused by Caudate Infarction Stephen Saris, MD \s=b\ An ischemic infarct in the caudate nucleus was associated with a contralateral chorea in a 47-year-old, hypertensive, diabetic man. To my knowledge, this is only the second report of isolated caudate infarction associated with chorea. Computed tomography demonstrated the basal ganglion lesion. (Arch Neurol 1983;40:590-591) IV/Tovement disorders can be pro¬ duced by infarction in the basal ganglia. Anatomic correlation has been limited to the 11 reported cases zine was refused. Over the ensuing six months there was diminution, but not dis¬ appearance, of his chorea. lesion, it was difficult to localize cho¬ rea or athetosis to a particular area of basal ganglion infarction. In the first case,1 an infarct in the caudate nucle¬ COMMENT us was There were two unusual features in this case. First, an ischemie infarction in the basal ganglia was associated with the sudden onset of a movement disorder. The Table describes 11 such patients with their pathologic find¬ ings. Each lesion was accompanied by choreoathetosis. Although the clinical disorder was contralateral to the correlated with a chorea. This patient's lesion was in the head of the caudate nucleus rather than in the anterior body, and she suffered from chorea of both the arm and leg. The second unusual feature is the CT demonstration of a lesion soon after the onset of chorea. Kase et al8 reported a CT-demonstrated infarct in the basal ganglia associated with of movement disorders in association with stroke.17 Postmortem examina¬ tions revealed infarcts in the contralateral basal ganglia. Findings of the autopsies, done weeks to years after the onset of the movement disorder, support a causal relationship. We report a case of infarction in which (1) the lesion, restricted to the head of the caudate nucleus and coro¬ na radiata, caused a contralateral chorea, and (2) computed tomographic (CT) scan was used to define the lesion at the time of the movement disor¬ der's onset. REPORT OF A CASE A 47-year-old, right-handed, hyperten¬ sive, diabetic man noted the sudden onset of "thick-tongued" speech associated with left-sided weakness. When examined, he had a mild dysarthria, weakness of the lower left part of the face, left (arm great¬ er than leg) hemiparesis, left hyperre¬ flexia, and left Babinski's sign. Chorea was evident in the left hand and wrist. A CT scan revealed a focal, hypodense lesion in the right corpus striatum involving the anterior body of the caudate nucleus and the corona radiata (Figure). On follow-up three months later, the patient's left-sided weakness had resolved, but the chorea was unchanged. Examina¬ tion revealed an involuntary, nonrhythmic, rapid flexion or extension of the metacarpophalangeal joints, with lesser involve¬ ment of the wrist and distal interphalan¬ geal joints. These movements could be suppressed, but not eliminated, by concen¬ tration or volitional movement. The chorea was unaffected by haloperidol (4 mg/day for three weeks), and a trial of perphena- Accepted for publication Dec 31, 1982. From the Department of Medicine, Division of Neurology, Duke University Medical Center, Durham, NC. Reprint requests to Box 31252, Duke University Medical Center, Durham, NC 27710 (Dr Saris). Computed tomographic scan slice (10 mm, 15° angle) after single injection of intravenous contrast material showed nonenhancing, rognded, low-density lesion, approximately 9 mm in diameter, in anterior aspect of body of right caudate nucleus encroaching on corona radiata." Autopsy-Confirmed Basal Ganglia Lesions Causing Contralateral Movement Disorders Source, yr Austregesilo and Galloni,' 1924 Von Steck,2 1926 Davison and Goodhart,3 1940 Basal Ganglion Lesion Infarct in R caudate nucleus (CN) Cyst in R globus pallidus (GP) and CN "Softening" in R CN; cyst in R putamen Clinical Findings L arm-leg chorea L arm-leg athetosis L arm-neck chorea Martin," 1957 Infarct in R GP L face-arm-leg chorea Denny-Brown,5 1962 Infarct in L putamen and R hand athetosis; Goldblatt et al,6 1974 Cyst in R putamen; L face-arm-leg chorea Dooling and Adams,7 1975 Infarct in L CN and R arm-hand athetosis CN R arm-leg dystonia infarct in R CN putamen Dooling and Adams,' 1975 Dooling and Adams,7 1975 Dooling and Adams,7 1975 Cavitation in L putamen and GP Infarction ¡ L putamen, GP. and CN Destruction in L CN and putamen Dooling and Adams,7 1975 Neuronal atrophy and gliosis in R CN and thalamus Downloaded From: http://archneur.jamanetwork.com/ by a University of Manitoba User on 06/04/2015 R arm-leg "involuntary spasms" R arm-leg-trunk "involuntary spasms" R neck-arm "involuntary jerking" L hand athetosis-dystonia the new onset of a movement disorder. Their patient had the onset of leftsided hemichorea-hemiballismus as¬ sociated with a right-sided, low-densi¬ ty lesion in the region of the putamen, anterior limb of internal capsule, and caudate nucleus. Massey et al9 and Yagnik and Dhopesh10 have reported four cases of asterixis following CT demonstration of ischemie or hemor¬ rhagic lesions in the basal ganglia. James Davis, MD, Wayne Massey, MD, and Dennis Osborne, MD, reviewed the manuscript. Nanci DeMarco and Don Powell provided techni¬ cal assistance. References 1. Austregesilo A, Gallotti O: Sur un cas d'hemipar\l=e'\sieet d'h\l=e'\michor\l=e'\eavec lesion du noyau caude. Rev Neurol 1924;1:41-43. 2. Von Steck H: Zur pathologischen Anatomie der echten posthemiplegischen Athetose. Schweiz. Arch Neurol Neurochir Psychiatr 1921; 8:75-84. 3. Davison C, Goodhart SP: Monochorea and somatotopic localization. Arch Neurol 1940; 43:792-803. 4. Martin JP: Hemichorea (hemiballismus) without lesions in the corpus Luysii. Brain 1957; 80:1-10. 5. Denny-Brown D: The Basal Ganglia. Oxford, England, Oxford University Press, 1962, pp 53-70, 105-121. 6. Goldblatt D, Markesbery W, Reeves AG: Recurrent hemichorea following striatal lesions. Arch Neurol 1974;31:51-54. 7. Dooling EC, Adams RD: The pathological anatomy of posthemiplegic athetosis. Brain 1975; 98:29-48. 8. Kase CS, Maulsby GO, deJuan E, et al: Hemichorea: Hemiballismus and lacunar infarction in the basal ganglia. Neurology 1981;31:452\x=req-\ 455. 9. Massey EW, Goodman JC, Stewart C, et al: Unilateral asterixis: Motor integrative dysfunction in focal vascular disease. Neurology 1979; 29:1180-1182. 10. Yagnik P, Dhopesh V: Unilateral asterixis. Arch Neurol 1981;38:601-602. 11. Matsui T, Hirano A: An Atlas of the Human Brain for Computerized Tomography. Tokyo, Igaku-Shoin Ltd, 1978, p 150. Trigeminal Sensory Neuropathy C. Miller Fisher, MD \s=b\ The etiology of trigeminal sensory neuropathy remains obscure. In a recent case, a relationship to herpes simplex virus might be inferred. A woman, aged 63 years, had at least ten episodes of "cold sore," always at the same site on her upper lip. After a typical prodromal burning, she expected a cold sore to appear, but a trigeminal sensory neuropathy began instead, starting at the site where the cold sores had always appeared. (Arch Neurol 1983;40:591-592) HPrigeminal sensory neuropathy, some 60 cases of which have been complete (40% of reported cases) to almost none. An oculosympathetic palsy and impairment of taste are commonly present. The motor compo¬ nent of the fifth nerve is almost always spared. Pain was present in the first stage of the illness in about one third of the reported cases, and trigeminal neuralgia may be a late complication. When recovery occurs, it may begin in three to six weeks or be long delayed. When the numbness spreads gradually, tumor of the base of the skull and of the trigeminal ganglion are the most serious differ¬ ential diagnoses. The cause of trigeminal sensory unknown. remains neuropathy reported,1 is a benign or self-limiting condition in which a creeping facial numbness spreads gradually in the territory of the trigeminal nerve, over a period of days, weeks, months, or years. The corresponding sensory def¬ icit varies from severe to slight. The regions involved in the reported cases were, in descending order of frequen¬ cy, divisions 1, 2, and 3; 2 and 3; 3 only; 2 only; and 1 and 2. The second and third divisions were involved about equally, twice as often as the first division. The condition was bilateral in four cases. Recovery varies from found the sensory root reduced to wisps of nerve tissue, and histological¬ ly there were collections of lympho¬ cytes. The state of the ganglion was not given in detail. Seward3 suggested an infective or toxic peripheral neuri¬ tis. Blau et al4 postulated a viral infec¬ tion and drew an analogy with Bell's palsy and benign abducens palsy. The case reported herein provides circum¬ stantial evidence of a relationship to herpes simplex virus. Accepted for publication Nov 26, 1982. From the Neurology Service, Massachusetts General Hospital, Boston. Reprint requests to Neurology Service, Massachusetts General Hospital, Boston, MA 02114 (Dr Fisher). A healthy woman, aged 63 years, was susceptible to "cold sores" and in the past 15 years had had at least ten bouts of herpes febrilis, which always came at the same site on the right side of the upper lip, about 2 cm from the midiine. Each cold Hughes,2 on surgical exploration, REPORT OF A CASE Downloaded From: http://archneur.jamanetwork.com/ by a University of Manitoba User on 06/04/2015 always preceded by tingling and burning for one to two days. At the beginning of the present illness, the patient experienced typical prodromal symptoms at the usual site. However, after three days, a surging, bubbling sensation sore was still present, and a cold sore did not patient noted "misperceptions," as though a hair or cobweb touched the right cheek. A few days later, pain appeared at the site of the expected cold sore and lancinating pains of an excruciat¬ ing severity began to occur in the right side of the upper gum. (From here on, all symptoms described are on the right side unless stated otherwise.) Herpes zoster was appear. The suspected. By day 16, pain had spread to the ala nasi, the side of the nose, the corner of the eye where the nosepiece of eyeglasses was would rest, the upper part of the cheek inferior to the orbit, and along a line running diagonally downwards from deep in the ear canal to the throat. The pains lasted slightly longer than a jab and were described as a pinch lasting a few seconds. When one pain ceased, there was respite for a few minutes before another occurred at an unrelated site. Each pain came with maximum intensity and disappeared with¬ out afterpain. Codeine sulfate was effec¬ tive. Pain involved the floor of the mouth along the lower gum and jaw and along the lateral edge of the tongue. At times, it felt as though the area were being lacerated by a fine razor blade or shards of glass. On day 17, the right part of the upper gum became numb. When the region was pricked by her physician, it felt dead. In the next ten days, numbness spread to the ala nasi, the side of the nose, the upper lip, the hard palate, the cheek inferior to the eye, the medial half of the upper eyelid,